2014
DOI: 10.1016/j.bbrc.2013.11.117
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The multiple expression of Ca2+-activated Cl− channels via homo- and hetero-dimer formation of TMEM16A splicing variants in murine portal vein

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Cited by 25 publications
(37 citation statements)
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“…At 24 -72 h after transfection, TMEM16A-expressing HEK293 cells elicited CaCC currents, which had characteristics consistent with those of our previous measurements (4). Neither the current density nor the kinetics (t act and t deact ) of CaCC currents were affected by the treatment with 1 mM cytochalasin D for 4 h in TMEM16A(abc)-and TMEM16A(acd)-HEK293 cells (n = 3 -6, P > 0.05; Fig.…”
Section: Short Communicationsupporting
confidence: 89%
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“…At 24 -72 h after transfection, TMEM16A-expressing HEK293 cells elicited CaCC currents, which had characteristics consistent with those of our previous measurements (4). Neither the current density nor the kinetics (t act and t deact ) of CaCC currents were affected by the treatment with 1 mM cytochalasin D for 4 h in TMEM16A(abc)-and TMEM16A(acd)-HEK293 cells (n = 3 -6, P > 0.05; Fig.…”
Section: Short Communicationsupporting
confidence: 89%
“…Recently, TMEM16A has been identified as a molecular component responsible for CaCC in various tissues (1 -3). TMEM16A is functionally expressed also in several VSMs including portal vein (4).…”
Section: Short Communicationmentioning
confidence: 99%
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“…-activated Cl 2 channel, with eight putative transmembrane domains and cytosolic N-and C-termini (Caputo et al, 2008;Schroeder et al, 2008;Yang et al, 2008), and functions as a dimer (Sheridan et al, 2011;Ohshiro et al, 2014). TMEM16A is located on chromosome 11q13, which is frequently amplified in many types of human cancer (Akervall et al, 1995;Huang et al, 2002), and plays an important role in driving the amplification of 11q13 (Komatsu et al, 2006).…”
mentioning
confidence: 99%